- Epigenetics Topics
This article provides insight into how your gene variants (or SNPs) affect your good gut bacteria and consequently how to digest and metabolise food to influence well being.
We are all familiar with the concept of evolution and how our ancestors adapted to survive and consequently shaped our appearance and our genetic heritage today. However, what we are less familiar with, it is the idea that the diet and their genetic adaptation, it was greatly influenced by the area they also lived in!
This element, in combination with natural selection, has played a crucial role in how our set of gene variants have emerged and shaped the evolution of the global modern human population.
A recent study published by Cornell University showed that farming communities established over 9,000 years ago in Europe modified their diets cultivating vegetables which led to genetic adaptations1,2.
Scientists found that specific dietary trends were present in the more favorable climate of particular areas, especially in the southern part of the continent1.
Researchers found by analysing ancient DNA, that populations that began to rely more on plant-based diets in the southern part of the European continent had better genetics.
Indeed, people who lived in a warmer climate, which made it easier for edible vegetation to grow and thrive like Italy and France, adapted with an “enhanced variant” of a gene called FADS11.
The FADS1 gene produces enzymes that play a vital role in the making of omega-3 and omega-6 long-chain polyunsaturated fatty acids (LCPUFA). Interestingly, while omega-3 and omega-6 LCPUFA can be obtained directly from animal-based diets, they are absent from plant-based foods.
Vegetarians require FADS1 enzymes to biosynthesise LCPUFA from short-chain fatty acids found in plants (roots, vegetables and seeds).
The FADS2 enzyme is also vital to convert plant omega-3 fatty acid into the active animal form of omega-3 known as EPA. This gene is more active in some people than others.
Our ancestral genes and their unique “variants’ or “alleles” play a significant role in the way our body may or may not absorb a specific type of food.
Some of these “ancient mutations” also called single nucleotide polymorphism (SNPs) may work better in synergism with our most loyal “Gut ally” – The Microbiome”.
This intricate network of trillions of microorganisms living in the digestive system, mainly bacteria, is a beautiful “powerhouse” that co-evolved with us and play a crucial role in :
- Digesting the food we eat5
- Absorbing & synthesising nutrients (good bacteria make for us Thiamine (B1), Riboflavin (B2), Pantothenic acid (B5), Pyridoxine (B6), Biotin (B7), Folates (B9), Cobalamin (B12), Vitamin K and more)5,6
- Defending us from harmful bacteria, viruses and other pathogens, essentially “Gut invaders” responsible for inflammation and Leaky Gut
- Immune regulation5
- Brain functions5
- Mood Regulation (Yes, the Microbiome produces essential “feel good and calming” neurotransmitters such as Seratonin and GABA!)4,5
Each of us has a specific type and number of bacteria that we host depending on several factors, including the genetics and health that we inhered from our parents5.
Unique gene variants (SNPs) from our paternal and maternal ancestors give us an insight into how we interact with our unique bacterial footprint.
The cooperative interaction between our gene products and the Good Bacteria is crucial for the right balance of our Microbiome.
For example, The human FUT2 gene (fucosyltransferase 2) may impact B12 absorption and the production of prebiotics in the Gut, to support the expansion of probiotics and the proper functioning and health of the Microbiome7.
A large number of our population (approx. 20%) carry a non-functional FUT2 gene called “non-secretory homozygous allele”. This non-functional FUT2 gene is unable to secrete a vital prebiotic that our body makes naturally to “feed” bifidobacteria that in return, help us to stay healthy7.
The FUT2 can contribute to the following Gut related diseases:
- Crohn’s disease8
- Celiac disease9
- Type 1 diabetes10
- Inflammatory bowel disease11
- Urinary tract infections (UTI)12
- B12 deficiency14
With a comprehensive gene testing system, we can identify the SNPs that are the most important for your digestion and food absorption (like FADS1, FADS2 described above).
We can “connect” the dots between your SNPs and your good bacteria. To provide advice on how you can improve your diet if you are genetically predisposed to have gut problems.
For example, if your FUT2 gene is unable to secrete prebiotics, we can help you to change this deficiency in effecting the Gut.
We will provide to you list of vegetable-based food combined with lifestyle changes, that will alleviate potential chronic conditions.
- Kaixiong Ye, Feng Gao, David Wang, Ofer Bar-Yosef, Alon Keinan. Dietary adaptation of FADS genes in Europe varied across time and geography. Nature Ecology & Evolution, 2017; 1: 0167 DOI: 1038/s41559-017-0167
- “Healthy diet? That depends on your genes.” Cornell University, ScienceDaily, 12 June 2017, sciencedaily.com/releases/2017/06/170612153554.htm>.
- “Single Nucleotide Polymorphisms in the FADS Gene Cluster Are Associated with Delta-5 and Delta-6 Desaturase445. Activities Estimated by Serum Fatty Acid Ratios.” PubMed Central (PMC) , ncbi.nlm.nih.gov/pmc/articles/PMC2903808/.
- “These bacteria may be the key to treating clinical depression” medicalxpress.com, 11 Dec 2018, https://medicalxpress.com/news/2018-12-bacteria-key-clinical-depression.html
- “What is the Gut Microbiome?” Food and Mood Centre, Deakin University, https://foodandmoodcentre.com.au/2016/07/what-is-the-gut-microbiome/
- Ian Rowland, Glen Gibson Kieran Tuohy “Gut microbiota functions: metabolism of nutrients and other food components” European J Nutr. 2018: 57(1): 1-24
- Secretor genotype (FUT2 gene) is strongly associated with the composition of Bifidobacteria in the human intestine. PLoS ONE. 2011;6(5):e20113.
- McGovern, D. P., Jones, M. R., Taylor, K. D., Marciante, K., Yan, X., Dubinsky, M., … & Rotter, J. I. (2010). Fucosyltransferase 2 (FUT2) non-secretor status is associated with Crohn’s disease. Human molecular genetics, 19(17), 3468-3476.
- Parmar, A. S., Alakulppi, N., Paavola‐Sakki, P., Kurppa, K., Halme, L., Färkkilä, M., … & Einarsdottir, E. (2012). Association study of FUT2 (rs601338) with celiac disease and inflammatory bowel disease in the Finnish population. Tissue antigens, 80(6), 488-493.
- Smyth, D. J., Cooper, J. D., Howson, J. M., Clarke, P., Downes, K., Mistry, T., … & Todd, J. A. (2011). FUT2 nonsecretor status links type 1 diabetes susceptibility and resistance to infection. Diabetes, 60(11), 3081-3084
- Hu D, Zhang D, Zheng S, Guo M, Lin X, et al. (2016) Association of Ulcerative Colitis with FUT2 and FUT3 Polymorphisms in Patients from Southeast China. PLOS ONE 11(1): e0146557. https://doi.org/10.1371/journal.pone.0146557
- Sheinfeld, J., Schaeffer, A. J., Cordon-Cardo, C., Rogatko, A., & Fair, W. R. (1989). Association of the Lewis blood-group phenotype with recurrent urinary tract infections in women. New England Journal of Medicine, 320(12), 773-777.
- Hurd, E. A., & Domino, S. E. (2004). Increased susceptibility of secretor factor gene Fut2-null mice to experimental vaginal candidiasis. Infection and immunity, 72(7), 4279-4281.
- Tanaka, T., Scheet, P., Giusti, B., Bandinelli, S., Piras, M. G., Usala, G., … & Ferrucci, L. (2009). Genome-wide association study of vitamin B6, vitamin B12, folate, and homocysteine blood concentrations. The American Journal of Human Genetics, 84(4), 477-482.
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